The Variation of Choroidal Thickness and Refractive Error after Cataract Surgery

PURPOSE: To evaluate the effect of cataract surgery on subfoveal choroidal thickness (SCT) and investigate the relationship between the variation of SCT and refractive error. METHODS: We retrospectively reviewed the medical records of 47 patients (47 eyes) who underwent uneventful phacoemulsification cataract surgery from March 2012 to February 2014. SCTs were measured using spectral-domain optical coherence tomography performed before surgery and at 1 month, 3 months and 6 months postoperatively. We investigated the differences in target refraction (TR) and postoperative spherical equivalent (SE), intraocular pressure (IOP) and central macular thickness (CMT) at all follow-ups. RESULTS: Compared with preoperative measurements, SCT showed a significant increase of 5.9 ± 13.3 µm at postoperative 1 month and 7.6 ± 18.1 µm at postoperative 3 months (p = 0.004 and p = 0.006, respectively), but no significant differences at postoperative 6 months (p = 0.104). The correlation between the variation of SCT and the differences in postoperative SE and TR were not significant at 1 month and 6 months, but were positively significant at 3 months (r = 0.310, p = 0.034). The variation of SCT showed no significant correlations with the postoperative change in IOP and CMT. CONCLUSIONS: SCT significantly increased up to 3 months after cataract surgery. The variation of SCT may affect the postoperative refractive error.

Nuclear Factor-kappa B Activation and Chemokine Genes Expression in HT-29 Intestinal Epithelial Cells in Response to Clostridium difficile Toxin A Stimulation

Intestinal epithelial cells are known to up-regulate the expression of several chemokines in response to bacterial toxins. Since there has been little understanding on the cellular mechanisms of C. difficile toxin A-induced mucosal inflammation, we investigated whether nuclear factor-kappa B (NF-kappaB) could regulate chemokine gene expression in HT-29 intestinal epithelial cells stimulated with C. difficile toxin A. C. difficile toxin A rapidly increased signals of NF-kappaB composed with p65 and p50 subunits in HT-29 cells, whereas it decreased the signals of IkappaBalpha. Blocking the NF-kB activation by transfection with dominant negative I kappa B alpha-containing retrovirus attenuated the upregulated expression of IL-8, GRO-alpha, and MCP-1 induced by C. difficile toxin A. These results suggest that NF-kappaB is a major regulator of chemokine gene expression in C. difficile toxin A-stimulated intestinal epithelial cells.